Immune microenvironment and immune cell dynamics in colitis-associated colorectal cancer: Mechanisms and therapeutic implications

Figure 1 Overview of the pathogenesis and treatment of colitis-associated colorectal cancer. This figure illustrates how gut microbiota dysbiosis, aberrant inflammatory signaling, and immune cell reprogramming collectively drive the evolutionary sequence of “inflammation-dysplasia-carcinogenesis”, while also highlighting current targeted therapeutic strategies. AMP: Antimicrobial peptide; JAK: Janus kinase; S1P: Sphingosine-1-phosphate; APE1/Ref-1: Apurinic/apyrimidinic endonuclease 1/redox factor-1; PD-1: Programmed death receptor 1; MSI: Microsatellite instability; NK: Natural killer; NF-κB: Nuclear factor-κB; STAT: Signal transducer and activator of transcription; PI3K: Phosphatidylinositol-3-kinase; AKT: Protein kinase B; CDK1: Cyclin-dependent kinase 1.